In Stock Cell Lines
Homo sapiens (Human)
Breast (mammary gland)
Adherent
The FSIP1 Knockout MDA-MB-231 Cell Line is a CRISPR/Cas9-engineered loss-of-function model targeting the oncogene FSIP1 in the aggressive triple-negative breast cancer cell line MDA-MB-231. FSIP1 disruption attenuates ??-catenin-dependent transcription and PI3K/AKT signalling, impairing key processes such as proliferation, migration, and chemoresistance. This ready-to-use knockout cell line facilitates mechanistic investigation of TNBC progression, Wnt/??-catenin pathway activity, and drug resistance mechanisms. Typical applications include TCF/LEF reporter assays, Transwell invasion, and drug sensitivity panels, making it a valuable resource for cancer biology and targeted therapy research.
LPCAT4 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG16478
LGMN Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG16099
ATP6V1C2 Knockout Hela Polyclonal Cells
Cat. No. ARG20967
DNAJC16 Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG39230
CIRBP Knockout 786-O Polyclonal Cells
Cat. No. ARG5589
Mouse Bronchial Smooth Muscle Cell Medium
Cat. No. ARM0424
The FSIP1 Knockout MDA-MB-231 Cell Line is a CRISPR/Cas9-edited knockout cell model designed to disrupt the FSIP1 gene, which encodes fibrous sheath-interacting protein 1, in a triple-negative breast cancer (TNBC) background. Generated on the MDA-MB-231 host using CRISPR/Cas9-mediated gene disruption, this loss-of-function system allows precise dissection of FSIP1’s oncogenic roles without specifying the exact editing outcome. By abolishing functional FSIP1 expression, the cell line provides a clean platform for mechanistic and translational research.
MDA-MB-231 is a human breast adenocarcinoma line derived from a metastatic pleural effusion, representing a classic TNBC model. It lacks ER, PR, and HER2 and harbours a TP53 mutation, driving its highly invasive and metastatic behaviour. Widely employed in cancer biology, these cells offer a stringent environment to study genes that control tumour progression and therapy resistance.
FSIP1 encodes fibrous sheath-interacting protein 1, an emerging oncogene in TNBC that promotes proliferation, migration, and chemoresistance. The protein integrates Wnt/??-catenin and PI3K/AKT signalling by interacting with ??-catenin, AKAP4, and GSK3??, and is transcriptionally regulated by TCF/LEF downstream of Wnt?CFrizzled receptors. FSIP1 knockout attenuates ??-catenin nuclear build-up, diminishing cyclin D1 and c-Myc expression, and dampens PI3K/AKT/mTOR and NF-??B activity. These concerted molecular changes impair the oncogenic signalling network.
In MDA-MB-231 cells, FSIP1 disruption is expected to blunt invasive, migratory, and colony-forming capacities while sensitizing cells to paclitaxel and doxorubicin. The model isolates FSIP1’s contribution to TNBC aggressiveness and drug tolerance, making it invaluable for exploring how loss of this gene rewires pathways and for identifying compensatory mechanisms or synthetic lethal interactions.
This knockout cell line supports a comprehensive suite of assays: Western blotting, RT-qPCR, TCF/LEF luciferase reporters, immunofluorescence for ??-catenin localization, colony formation, wound healing, Transwell invasion, apoptosis (Annexin V), and drug sensitivity testing. Applications span mechanistic dissection of Wnt-dependent transcription, drug resistance profiling, and transcriptomic analysis via RNA-seq, enabling the discovery of FSIP1-dependent gene networks. It thus serves as a versatile tool for TNBC research and therapy development. For further information, contact Ascent Research.
